scholarly journals Feeding Soy Protein Isolate andor Omega-3 Polyunsaturated Fatty Acids on the Spleen-Liver Axis in a Female Rat Model of Autosomal Recessive Polycystic Kidney Disease with Liver Steatosis

2016 ◽  
Author(s):  
Lauren Gibson
Keyword(s):  
Fatty Acids ◽  
Kidney Disease ◽  
Soy Protein ◽  
Autosomal Recessive ◽  
Liver Steatosis ◽  
Soy Protein Isolate ◽  
Protein Isolate ◽  
Female Rat ◽  
Omega 3 ◽  
Polycystic Kidney

scholarly journals Effects of Diet Containing Soy Protein Isolate on Liver Metabolic Methylation Status Using Obese Zucker Rat Model (P08-033-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Reza Hakkak ◽  
Soheila Korourian ◽  
Oleksandra Pavliv ◽  
Stepan Melnyk
Keyword(s):  
Rat Model ◽  
Soy Protein ◽  
Methylation Status ◽  
Liver Steatosis ◽  
Soy Protein Isolate ◽  
The United States ◽  
Protein Isolate ◽  
Zucker Rats ◽  
Zucker Rat ◽  
Obese Zucker Rat

Abstract Objectives The obesity epidemic is continuing to grow in the United States and world for past two decades. There is a link between obesity and chronic diseases development such as diabetes, cardiovascular disease, certain types of cancer and liver diseases. Previously, we reported that obesity caused a significant increase liver steatosis and feeding soy protein isolate (SPI) reduced liver steatosis. The mechanism of SPI protection against liver steatosis is less known. We hypothesize that soy protein diet will reduce development of liver steatosis caused by obesity in part by changing methylation status. The objective of the present study was to investigate the effects of SPI feeding on liver metabolic methylation status using obese zucker rat model. Methods After one week of acclimation, five weeks old female lean and obese Zucker rats (n = 8/group) were randomly fed AIN-93-G diet with either casein (CAS as control) or SPI as source of protein for 22 weeks. Rats were weighted twice per week. Liver sample metabolites concentrations were measured using HPLC with Electrochemical Detection and LC-MS. Results Our results shows that; 1) obesity increased body weight significantly (P < 0.001) for both CAS and SPI diets; 2) Obese SPI-fed rats significantly (P < 0.001) reduced liver steatosis compared to obese CAS-fed rats. Also, our results show that liver metabolic profile in lean SPI-fed rats significantly (P < 0.025) increased SAM/SAH ratio (methylation ratio) compare to CAS-fed rats. Obese SPI-fed rats significantly (P < 0.001) decrease level of Homocysteine in liver and increase significantly (P < 0.001) Methionine/Homocysteine ratio. Conclusions In summary we showed that SPI diet can reduce liver steatosis by changing methylation status and improved metabolism of Homocysteine, toxic intracellular compound, through remethylation to Methionine. Funding Sources Arkansas Children's Research Institute's University Medical Group Fund grant program and Arkansas.

scholarly journals Long-Term Soy Protein Isolate Consumption Reduces Liver Steatosis Through Changes in Global Transcriptomics in Obese Zucker Rats

2020 ◽  
Vol 7 ◽  
Author(s):  
Melisa Kozaczek ◽  
Walter Bottje ◽  
Byungwhi Kong ◽  
Sami Dridi ◽  
Diyana Albataineh ◽  
...  
Keyword(s):  
Regression Analysis ◽  
Soy Protein ◽  
Liver Steatosis ◽  
Soy Protein Isolate ◽  
Protein Isolate ◽  
Differentially Expressed ◽  
Zucker Rats ◽  
Obese Zucker Rats ◽  
Upstream Regulators

To determine how soy protein isolate (SPI) ameliorated liver steatosis in male obese Zucker rats, we conducted global transcriptomic expression (RNAseq) analysis on liver samples of male rats fed either the SPI or a control casein (CAS)-based diet (n = 8 per group) for 16 weeks. Liver transcriptomics were analyzed using an Ilumina HiSeq system with 2 × 100 base pair paired-end reads method. Bioinformatics was conducted using Ingenuity Pathway Analysis (IPA) software (Qiagen, CA) with P &lt; 0.05 and 1.3-fold differential expression cutoff values. Regression analysis between RNAseq data and targeted mRNA expression analysis of 12 top differentially expressed genes (from the IPA program) using quantitative PCR (qPCR) revealed a significant regression analysis (r2 = 0.69, P = 0.0008). In addition, all qPCR values had qualitatively similar direction of up- or down-regulation compared to the RNAseq transcriptomic data. Diseases and function analyses that were based on differentially expressed target molecules in the dataset predicted that lipid metabolism would be enhanced whereas inflammation was predicted to be inhibited in SPI-fed compared to CAS-fed rats at 16 weeks. Combining upstream regulator and regulator effects functions in IPA facilitates the prediction of upstream regulators (e.g., transcription regulators) that could play important roles in attenuating or promoting liver steatosis due to SPI or CAS diets. Upstream regulators that were predicted to be activated (from expression of down-stream targets) linked to increased conversion of lipid and transport of lipid in SPI-fed rats included hepatocyte nuclear factor 4 alpha (HNF4A) and aryl hydrocarbon receptor (AHR). Upstream regulators that were predicted to be activated in CAS-fed rats linked to activation of phagocytosis and neutrophil chemotaxis included colony stimulating factor 2 and tumor necrosis factor. The results provide clear indication that long-term SPI-fed rats exhibited diminished inflammatory response and increased lipid transport in liver compared to CAS-fed rats that likely would contribute to reduced liver steatosis in this obese Zucker rat model.

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